SV40 and Cellular Gene Expression in the Maintenance of the Tumorigenic Syndrome

Pollack, Robert; Lo, Angela Kwok Fung; Steinberg, Bettie M.; Smith, Karla R.; Shure, Helen; Blanck, George; Verderame, Michael F.

doi:10.1101/sqb.1980.044.01.072

Cited by 13 publications

(13 citation statements)

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“…In addition, altered cells with an increased capacity for colony formation in agar and tumor production in animals eventually dominate the cultured population. Data (9,18,28), susceptibility to growth control by the environment in the animal (3,12,15,24), and susceptibility to immune surveillance (5,8,14,16). Alterations in each parameter may not occur simultaneously nor follow a predictable pathway.…”

Section: Discussionmentioning

confidence: 99%

“…This process, termed the progression of tumorigenicity, results in a steady increase in tumor malignancy as the cells with increased growth advantage gradually predominate (11,13). To determine what parameters affect the growth and metastatic properties of tumor cells, much research has focused on in vitro cell lines that vary in their tumorigenic capacities (6,9,14,16,(18)(19)(20)27). Most of these cell lines represent variants of fully malignant cell lines that have been adapted to grow in culture.…”

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confidence: 99%

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Progression of the transformed phenotype in clonal lines of Abelson virus-infected lymphocytes.

Whitlock¹,

Ziegler²,

Witte³

1983

Mol. Cell. Biol.

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Some molecular changes which correlate with the tumorigenic progression of neoplastic cells can best be studied with in vitro cell lines that represent each stage in the progression. Lymphoid cells infected by Abelson murine leukemia virus exhibit a wide range of growth potential in vitro and in vivo. Uncloned populations that are poorly oncogenic early after infection become progressively more oncogenic with successive passages of the cells in culture. In such mass cultures, it is difficult to evaluate whether a rare subpopulation of highly oncogenic cells becomes dominant in the culture or whether the individual cells progress in oncogenic phenotype. To examine this latter possibility, Abelson virus-infected lymphoid cells were cloned by limiting-dilution culture 10 days postinfection. We isolated two clones that grew poorly in agar, required feeder layers of adherent bone marrow cells for growth in liquid culture, and were extremely slow to form tumors in syngeneic animals. Both clones, after passage in the presence of adherent feeder layers for 3 months, grew well in liquid and agar-containing cultures in the absence of feeder layers and formed tumors in animals at a rapid rate. The progression of these clonal cell lines to a more malignant growth phenotype occurred in the absence of detectable changes in the concentration, half-life, phosphorylation, in vitro kinase activity, or cell localization of the Abelson virus-encoded transforming protein. No change in the concentration or arrangement of integrated Abelson viral DNA sequences was detected in either clone. Thus, perhaps changes in the expression of cellular genes would appear to alter the growth properties of lymphoid cells after their initial transformation by Abelson virus. Such cellular changes could complement the activity of the Abelson virus transforming protein in producing the fully malignant growth phenotype.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Progression of the transformed phenotype in clonal lines of Abelson virus-infected lymphocytes.

Whitlock¹,

Ziegler²,

Witte³

1983

Mol. Cell. Biol.

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“…It contains neither of the early SV40 viral proteins [24] . It is clear that, while FI' 1-4 is non-tumorigenic, it can give rise to a tumorigenic variant.…”

Section: Discussionmentioning

confidence: 99%

Tumorigenicity of revertants from an SV40‐transformed line

et al. 1979

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A syndrome of in vitro properties correlates with the tumorigenicity of SV40-transformed rodent cells. These properties are: plasminogen activator production, loss of large actin cables, and anchorage-independent growth. An established rat fibroblast line, its SV40 transformant, several T-antigen negative revertants, and a spontaneous retransformant isolated from one of the revertants were analyzed in vivo for their tumorigenicity and in vitro for the syndrome. The two transformed lines were highly tumorigenic, and had clearly abnormal in vitro properties. The parental rat line was weakly tumorigenic in nude mice and demonstrated a slightly transformed response in the in vitro assays. The revertants were completely nontumorigenic. Expression of the in vitro syndrome was not uniform for all revertants; however, most cell lines maintained the correlation of the syndrome and tumorigenicity.

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“…Rat postcrisis lines have been described (12,13). They were grown in Dulbecco's modified Eagle's medium supplemented with penicillin (100 units/ml), streptomycin (100,ug/ml), and 10% fetal calf serum (Rehatuin).…”

Section: Methodsmentioning

confidence: 99%

“…Perhaps in those cell lines the F-actin perturbation is maintained by transformation-specific molecules coded for by the host cell. We have recently shown that a 54,000-dalton protein is present in large amounts in 14B and MCA but in much smaller amounts in Rat 1 and the 14B revertants and is absent from precrisis rat fibroblasts (13).…”

mentioning

confidence: 96%

Cytoskeletal F-actin patterns quantitated with fluorescein isothiocyanate-phalloidin in normal and transformed cells.

Verderame¹,

Alcorta²,

Egnor³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

152

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Actin in cultured fibroblasts is organized into a complex set of fibers. Patterns of organization visualized with antibody to actin are similar but not identical to those visualized with fluorescein isothiocyanate-phalloidin (Fl-phalloidin), a chemical that binds to F-actin polymer with a dissociation constant of 2.7 X 10(-7) M [Wulf, E., Deboben, A., Bautz, F. A., Faulstich, H. & Wieland, T. (1979) Proc. Natl. Acad. Sci. USA 76, 4498-4502]. Fl-phalloidin reveals that transformed cells have fewer, finer, and shorter F-actin-containing structures than do normal cells. Two-color fluorescence microscopy of single cells reveals that F-actin staining by Fl-phalloidin picks out the cytoskeletal cables more sharply than does antibody to actin, due to a reduced intracellular background fluorescence. This improved resolution permits sorting of cellular Fl-phalloidin patterns into four classes ranging in organization from 90% of the cytoplasm occupied by large cables to the absence of detectable cables. Reproducible differences in pattern distributions between normal and transformed cell lines have been quantitated. Fl-phalloidin together with rhodamine-based indirect antibody to simian virus 40 tumor antigen reveals a direct relationship between the degree of pattern change and simian virus 40 nuclear antigen expression in intermediate transformed 3T3 cell lines [Risser, R. & Pollack, R. (1974) Virology 59, 477-489].

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SV40 and Cellular Gene Expression in the Maintenance of the Tumorigenic Syndrome

Cited by 13 publications

References 0 publications

Progression of the transformed phenotype in clonal lines of Abelson virus-infected lymphocytes.

Progression of the transformed phenotype in clonal lines of Abelson virus-infected lymphocytes.

Tumorigenicity of revertants from an SV40‐transformed line

Cytoskeletal F-actin patterns quantitated with fluorescein isothiocyanate-phalloidin in normal and transformed cells.

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